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Etiology and Morphogenesis of Congenital Heart Disease : From Gene Function and Cellular Interaction to Morphology.

Bibliographic Details
Main Author: Nakanishi, Toshio.
Other Authors: Markwald, Roger R., Baldwin, H. Scott., Keller, Bradley B., Srivastava, Deepak., Yamagishi, Hiroyuki.
Format: eBook
Language:English
Published: Tokyo : Springer Japan, 2016.
Edition:1st ed.
Subjects:
Electronic books.
Online Access:Click to View
Table of Contents:
  • Intro
  • Preface
  • Contents
  • Part I: From Molecular Mechanism to Intervention for Congenital Heart Diseases, Now and the Future
  • Perspective
  • 1: Reprogramming Approaches to Cardiovascular Disease: From Developmental Biology to Regenerative Medicine
  • 1.1 Introduction
  • 1.2 Molecular Networks Regulate Cardiac Cell Fate
  • 1.3 Cardiac Fibroblasts in the Normal and Remodeling Heart
  • 1.4 Direct Cardiac Reprogramming In Vitro
  • 1.5 Direct Cardiac Reprogramming In Vivo
  • 1.6 Direct Cardiac Reprogramming in Human Fibroblasts
  • 1.7 Challenges and Future Directions
  • References
  • 2: The Arterial Epicardium: A Developmental Approach to Cardiac Disease and Repair
  • 2.1 Origin of the Epicardium
  • 2.2 Epicardium-Derived Cells (EPDCs)
  • 2.3 Heterogeneity of Epicardial Cells
  • 2.3.1 The Cardiac Fibroblast
  • 2.3.2 Arterial Smooth Muscle Cell
  • 2.3.3 Endothelial Cells
  • 2.3.4 Cardiomyocytes
  • 2.3.5 The Purkinje Fiber
  • 2.4 Congenital and Adult Cardiac Disease
  • 2.4.1 Non-compaction
  • 2.4.2 Conduction System Anomalies
  • 2.4.3 Valvulopathies
  • 2.4.4 Coronary Vascular Anomalies
  • 2.5 Cardiovascular Repair
  • 2.6 Future Directions and Clinical Applications
  • References
  • 3: Cell Sheet Tissue Engineering for Heart Failure
  • 3.1 Introduction
  • 3.2 Cell Sheet Engineering
  • 3.3 Cardiac Tissue Reconstruction
  • 3.4 Cell Sheet Transplantation in Small Animal Models
  • 3.5 Cell Sheet Transplantation in Preclinical and Clinical Studies
  • 3.6 Conclusions
  • References
  • 4: Future Treatment of Heart Failure Using Human iPSC-Derived Cardiomyocytes
  • 4.1 Introduction
  • 4.2 Cardiac Differentiation from Human iPSCs
  • 4.3 Nongenetic Methods for Purifying Cardiomyocytes
  • 4.4 Transplantation of Human PSC-Derived Cardiomyocytes
  • 4.5 Future Directions
  • References
  • 5: Congenital Heart Disease: In Search of Remedial Etiologies.
  • 5.1 Introduction
  • 5.1.1 Emerging Concepts
  • 5.1.2 Hub Hypothesis
  • 5.2 Searching for Candidate Signaling Hubs in Heart Development
  • 5.2.1 Nodal Signaling Kinases
  • 5.2.2 Filamin A
  • 5.2.3 Relevance of Signaling Hubs to CHD
  • 5.3 Lineage Is a Key to Remedial Therapy
  • 5.3.1 Postnatal Origin of Cardiac Fibroblasts
  • 5.3.2 A Strategy to Use Fibroblast Progenitors to Carry Genetic Payloads
  • 5.3.2.1 This Strategy Calls for a Conceptual Revision in Our Thinking About Fibroblasts
  • 5.4 Remedial Therapies: Delivering Genetic ``Payloads ́́
  • 5.4.1 Preliminary Studies
  • References
  • Part II: Left-Right Axis and Heterotaxy Syndrome
  • 6: Left-Right Asymmetry and Human Heterotaxy Syndrome
  • 6.1 Introduction
  • 6.2 Molecular and Cellular Mechanisms of Left-Right Determination
  • 6.2.1 Node Cell Monocilia Create Leftward ``Nodal Flow ́́and Activate Asymmetry Signaling Around the Node
  • 6.2.2 Asymmetry Signaling Transmits to the Left Lateral Plate Mesoderm
  • 6.2.3 Genes Associated with the Human Heterotaxy Syndrome
  • 6.3 Clinical Manifestation of the Heterotaxy Syndrome
  • 6.3.1 Right Isomerism
  • 6.3.2 Left Isomerism
  • 6.4 Long-Term Prognosis of Heterotaxy Patients
  • 6.4.1 Protein-Losing Enteropathy
  • 6.4.2 Arrhythmias
  • 6.4.3 Heart Failure
  • 6.4.4 Hepatic Dysfunction
  • 6.4.5 Management of Failing Fontan Patients
  • 6.5 Future Direction and Clinical Implications
  • References
  • 7: Roles of Motile and Immotile Cilia in Left-Right Symmetry Breaking
  • 7.1 Introduction
  • 7.2 Symmetry Breaking by Motile Cilia and Fluid Flow
  • 7.3 Sensing of the Fluid Flow by Immotile Cilia
  • 7.4 Readouts of the Flow
  • 7.5 Future Directions
  • References
  • 8: Role of Cilia and Left-Right Patterning in Congenital Heart Disease
  • 8.1 Introduction
  • 8.1.1 Heterotaxy, Primary Ciliary Dyskinesia, and Motile Cilia Defects.
  • 8.1.2 Motile Respiratory Cilia Defects in Other Ciliopathies
  • 8.1.3 Ciliary Dysfunction in Congenital Heart Disease Patients with Heterotaxy
  • 8.1.4 Respiratory Complications in Heterotaxy Patients with Ciliary Dysfunction
  • 8.1.5 Left-Right Patterning and the Pathogenesis of Congenital Heart Disease
  • 8.1.6 Ciliome Gene Enrichment Among Mutations Causing Congenital Heart Disease
  • 8.1.7 Ciliary Dysfunction in Congenital Heart Disease Patients Without Heterotaxy
  • 8.1.8 Future Directions and Clinical Implications
  • References
  • 9: Pulmonary Arterial Hypertension in Patients with Heterotaxy/Polysplenia Syndrome
  • References
  • Perspective
  • Part III: Cardiomyocyte and Myocardial Development
  • 10: Single-Cell Expression Analyses of Embryonic Cardiac Progenitor Cells
  • 10.1 Introduction
  • 10.2 CPCs of the Two Heart Fields
  • 10.3 CPC Specification
  • 10.4 The Potential of Single-Cell Transcriptomics in the Study of CPC Specification
  • 10.5 Future Direction and Clinical Implication
  • References
  • 11: Meis1 Regulates Postnatal Cardiomyocyte Cell Cycle Arrest
  • 11.1 Introduction
  • 11.2 Results
  • 11.2.1 Expression of Meis1 During Neonatal Heart Development and Regeneration
  • 11.2.2 Cardiomyocyte Proliferation Beyond Postnatal Day 7 Following Meis1 Deletion
  • 11.2.3 MI in Meis1 Overexpressing Heart Limits Neonatal Heart Regeneration
  • 11.2.4 Regulation of Cyclin-Dependent Kinase Inhibitors by Meis1
  • 11.3 Future Direction and Clinical Implications
  • References
  • 12: Intercellular Signaling in Cardiac Development and Disease: The NOTCH pathway
  • 12.1 Introduction
  • 12.2 Left Ventricular Non-compaction (LVNC)
  • 12.3 The NOTCH Signaling Pathway
  • 12.4 NOTCH in Ventricular Chamber Development
  • 12.5 Future Directions and Clinical Implications
  • References.
  • 13: The Epicardium in Ventricular Septation During Evolution and Development
  • 13.1 Introduction
  • 13.2 Septum Components in the Completely Septated Heart
  • 13.3 The Presence of the Epicardium in Amniotes
  • 13.4 The Epicardium in the Avian Heart
  • 13.5 Disturbance of the Epicardium
  • 13.6 Septum Components in Reptilian Hearts
  • 13.7 Tbx5 Expression Patterns
  • 13.8 Discussion
  • References
  • 14: S1P-S1p2 Signaling in Cardiac Precursor Cells Migration
  • References
  • 15: Myogenic Progenitor Cell Differentiation Is Dependent on Modulation of Mitochondrial Biogenesis through Autophagy
  • 16: The Role of the Thyroid in the Developing Heart
  • References
  • Perspective
  • Part IV: Valve Development and Diseases
  • 17: Atrioventricular Valve Abnormalities: From Molecular Mechanisms Underlying Morphogenesis to Clinical Perspective
  • 17.1 Introduction
  • 17.2 RV-TV Dysplastic Syndrome
  • 17.2.1 Anatomic Features of the Heart in Ebsteinś Anomaly Patients
  • 17.2.2 Morphogenetic Features of the Heart in Patients with Uhlś Anomaly
  • 17.2.3 Absence of the TV
  • 17.3 Bone Morphogenetic Proteins (BMPs) and Their Important Role in Cushion Formation
  • 17.3.1 Role of BMP2 in Cushion Mesenchymal Cell (CMC) Migration
  • 17.3.2 BMP2 Induces CMC Migration and Id and Twist Expression
  • 17.3.3 BMP2 Induces Expression of ECM Proteins in the Post-EMT Cushion
  • 17.4 The Role of BMP2 for Cardiomyocytes Formation
  • 17.5 Future Direction
  • References
  • 18: Molecular Mechanisms of Heart Valve Development and Disease
  • 18.1 Introduction
  • 18.2 Heart Valve Development
  • 18.3 Heart Valve Disease
  • 18.3.1 Calcific Aortic Valve Disease (CAVD)
  • 18.3.2 Myxomatous Valve Disease
  • 18.4 Signaling Pathways in Heart Valve Development and Disease
  • 18.5 Future Directions and Clinical Implications
  • References.
  • 19: A Novel Role for Endocardium in Perinatal Valve Development: Lessons Learned from Tissue-Specific Gene Deletion of the Tie...
  • 19.1 Introduction
  • 19.2 Model for Valvar Endocardial-Specific Gene Deletion
  • 19.3 Tie1 Is Required for Late-Gestational and Early Postnatal Aortic Valve Remodeling
  • 19.4 Future Directions
  • References
  • 20: The Role of the Epicardium in the Formation of the Cardiac Valves in the Mouse
  • 20.1 Introduction
  • 20.1.1 The AV Valves and Their Leaflets
  • 20.1.2 The Epicardium and Epicardially Derived Cells (EPDCs)
  • 20.1.3 The Contribution of EPDCs to the Developing AV Valves
  • 20.2 The Role of Bmp Signaling in Regulating the Contribution of EPDC to the AV Valves
  • 20.2.1 Epicardial-Specific Deletion of the Bmp Receptor BmpR1A/Alk3 Leads to Disruption of AV Junction Development
  • 20.2.2 Discussion
  • 20.2.3 Future Direction and Clinical Implications
  • References
  • 21: TMEM100: A Novel Intracellular Transmembrane Protein Essential for Vascular Development and Cardiac Morphogenesis
  • References
  • 22: The Role of Cell Autonomous Signaling by BMP in Endocardial Cushion Cells in AV Valvuloseptal Morphogenesis
  • References
  • Perspective
  • Part V: The Second Heart Field and Outflow Tract
  • 23: Properties of Cardiac Progenitor Cells in the Second Heart Field
  • 23.1 Introduction
  • 23.2 Demarcating the First and Second Heart Fields and Their Contributions to the Heart
  • 23.3 New Insights into the Role and Regulation of Noncanonical Wnt Signaling in the Second Heart Field and the Origins of Cono...
  • 23.4 Involvement of the Second Heart Field in Atrial and Atrioventricular Septal Defects
  • 23.5 Future Directions and Clinical Implications
  • References
  • 24: Nodal Signaling and Congenital Heart Defects
  • 24.1 Introduction
  • 24.2 The Nodal Signaling Pathway
  • 24.3 Requirement for Nodal in Development.
  • 24.4 Congenital Heart Defects Associated with Perturbations in Nodal Signaling.

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